Study on myocardial injury of rats induced by yunaconitine through mitochondrial apoptosis pathway
- VernacularTitle:滇乌碱通过线粒体凋亡途径致大鼠心肌损伤的研究
- Author:
Ying SITU
1
;
Wanqiu CHENG
1
;
Zhibin SHEN
1
;
Yanfen CHEN
1
;
Chunping TANG
1
;
Cong CHEN
1
;
Tao JIANG
2
Author Information
1. School of Traditional Chinese Medicine，Guangdong Pharmaceutical University，Guangzhou 510006，China
2. Laboratory Animal Center，Guangdong Pharmaceutical University，Guangzhou 510006，China
- Publication Type:Journal Article
- Keywords:
yunaconitine;
cardiotoxicity;
oxidative stress
- From:
China Pharmacy
2022;33(23):2864-2868
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To study the effects of yunaconitine on myocardial injury in rats and its mechanism related to mitochondrial apoptosis pathway rats. METHODS Forty SD rats were divided into normal group （normal saline）， yunaconitine high-dose and low-dose groups（0.14， 0.09 mg/kg）and aconitine group （positive control， 0.88 mg/kg） by random number method， with 10 rats in each group. They were given relevant medicine intragastrically， once a day， for consecutive 7 days. The levels of lactate dehydrogenase （LDH）， creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， superoxide dismutase （SOD） and malondialdehyde （MDA） in serum as well as the level of reactive oxygen species （ROS） in myocardial tissue were detected. The pathomorphological changes of myocardium and ultrastructural changes of myocardial mitochondria were all observed. The apoptosis of cardiomyocytes was determined. The protein relative expressions of B-cell lymphoma-2 （Bcl-2）， Bcl-2 associated X protein （Bax）， caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 were determined in myocardium of rats. RESULTS Compared with normal group， the serum levels of LDH， CK， CK-MB and MDA， the apoptotic numbers of cardiomyocytes， the level of ROS and protein expression of caspase-3 in myocardium were increased significantly in yunaconitine high-dose and low- dose groups （P＜0.05 or P＜0.01）； serum level of SOD and Bcl-2/Bax ratio in myocardium were all decreased significantly （P＜ 0.01）； the protein relative expressions of caspase-9， cleaved-caspase-9， caspase-3 and cleaved-caspase-3 in myocardium were significantly increased in yunaconitine high-dose group （P＜0.05）； some pathomorphological changes were found in 2 groups， such as myocardial fiber disorder， mitochondrial swelling. CONCLUSIONS Yunacotine could cause myocardial injury in rats. Its mechanism might be related to destroying the integrity of cardiomyocyte membrane， causing oxidative stress of cardiomyocyte， and inducing the apoptosis of myocardial cells through mitochondrial pathway.
